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Horses

Interstitial Pneumonia

Interstitial pneumonia is an uncommon cause of acute or chronic disorders of the lower respiratory tract of horses. However, because of the severity of the process, recognition and definitive diagnosis of this entity are important as early as possible in its clinical course.

The term interstitial pneumonia defines a number of diseases that are chronic and progress to pulmonary fibrosis. The course is insidious and morphologically characterized by alveolar structural derangements that lead to loss of functional gas exchange units of the lung and altered mechanical properties of the lung, characterizing the pneumonia as a restrictive lung problem.

Etiology of Interstitial Pneumonia

Pathophysiology of Interstitial Pneumonia

Interstitial pneumonia progresses through four phases. During the first, the initial insult causes parenchymal injury and alveolitis. This is followed by a proliferative phase characterized by cellular and parenchymal alterations in tissues of the lung. Chronic cases progress to the development of interstitial fibrosis, whereas the final stage results in end-stage irreparable fibrosis of the lung.

The structural changes that occur in the lung reduce the number of functional alveoli, adversely affecting ventilatory function of the lung and altering ventilation/per-fusion relationships. Reduced lung compliance is associated with the loss of distensible alveoli and presence of pulmonary edema and fibrosis. Total and vital lung capacities are decreased in association with the loss of functional gas exchange units and reduced lung compliance. The work of breathing is increased, resulting in exercise intolerance and difficulty in breathing. Pulmonary hypertension and cor pulmonale may present as complications of interstitial pneumonia and fibrosis. Although the origin of pulmonary hypertension is unclear, hypoxic vasoconstriction and generation of vasoactive compounds (such as endothelin-1) that alter pulmonary vascular resistance acutely, and vessel anatomy chronically, may play a role.

Interstitial Pneumonia: Clinical Signs

Horses affected with interstitial pneumonia frequently present with fever, cough, weight loss, nasal discharge, exercise intolerance, severe dyspnea, cyanosis, and a restrictive breathing pattern. A “heave line” is frequently present; nostril flare and an anxious expression are usual. The history can be acute or chronic. Although affected foals are frequently depressed and anorectic, adults may be bright and alert with a variable appetite. The disease proceeds toward death in many cases, with progressive respiratory compromise, although some also may improve slowly with time. More than one foal at a farm may be affected.

Diagnosis of Interstitial Pneumonia

In older horses, the primary differential diagnosis of heaves may be excluded by the leukocytosis and hyperfibrinogenemia that commonly occur in horses with interstitial pneumonia and fibrosis but do not occur in horses with heaves. However, these abnormal features are common in horses with infectious bronchopneumonia and thoracic radiography is paramount in the establishment of a definitive diagnosis. Typically, thoracic radiographs reveal extensive interstitial and bronchointerstitial pulmonary patterns (). Nodular infiltrates may be present, either large or miliary, but always diffusely distributed.

Culture of transtracheal or bronchoalveolar lavage (bronchoalveolar lavage) aspirates often yields no significant growth of bacterial or fungal pathogens. This is particularly useful in foals and, in combination with negative results of a Gram-stained tracheal aspirate, reinforces the clinical diagnosis of interstitial pneumonia. Cytologic evaluation of tracheal or bronchoalveolar lavage fluid shows increased numbers of neutrophils and macrophages. If P. carinii is involved, bronchoalveolar lavage fluid may reveal trophozoites or intracystic bodies with special stains, such as toluidine blue or methenamine silver.

Histologic examination of a transthoracic lung biopsy specimen is the definitive diagnostic test for chronic interstitial pneumonia and fibrosis (). Care must be taken to ensure the biopsy is obtained from a representative area and ultrasound guidance has been useful in the hands of the author. Complications from this technique are uncommon but can occur. Biopsy rarely defines the causative agent but confirms the clinical diagnosis.

Additional diagnostics could include arterial blood gas analysis, abdominocentesis, and thoracocentesis to rule out metastatic neoplastic disease, pulmonary function testing, viral isolation, serologic testing for antibody to fungi and chicken serum if hypersensitivity pneumonitis is suspected, and immunohistochemical evaluation of lung tissue for suspected infectious agents. A complete cardiac evaluation also should be conducted to screen for pulmonary hypertension and cor pulmonale.

Treatment of Interstitial Pneumonia

Treatment of these cases is often unrewarding. Therapeutic goals are treatment of any underlying or secondary infection; suppression of inflammation; maintenance of tissue oxygen delivery within appropriate limits; relief of any associated bronchoconstriction; and prevention or treatment of complications. Environmental control, with appropriate temperature and humidity control and good ventilation, is beneficial.

Parenteral corticosteroid therapy is the mainstay of treatment, with early and aggressive therapy providing the best long-term outcome, particularly in foals. In one report of 23 foals affected with acute bronchointerstitial pneumonia, 9 of 10 treated with corticosteroids survived, whereas none of those not receiving steroid treatment lived. Dexamethasone (0.1 mg/kg q24h) is suggested initially. Inhaled beclomethasone (8 μg/kg q12h) may be considered. Additional antiinflammatory therapy includes, but is not limited to, dimethyl sulfoxide (DMSO; 1 g/kg as a 10% solution IV q24h), flunixin meglumine (Banamine; 1 mg/kg IV q12h) and methyl sulfonyl methane (15-20 mg/kg PO q24h).

Broad-spectrum antimicrobial treatment should be instituted initially, particularly in foals, as described for the treatment of infectious bronchopneumonia (see “Pleuropneumonia”). The choice of antimicrobial and duration of therapy should be dictated finally by the culture and sensitivity results from the transtracheal aspirate and by the patient’s clinical course.

Foals, in particular, and adults with severe respiratory distress may benefit from nasal insufflation of humidified oxygen, with flow rates of 10 L/min for foals and 15 L/min in adults. If necessary, as determined by persistent hypoxemia in the face of intranasal insufflation at the rates given, a second nasal canula can be placed in the opposite nostril to increase the Fio2. Care must be taken to avoid obstruction of the nasal passages. Alternatively, intratracheal or transtracheal insufflation can be considered to further increase Fio2 and improve oxygenation.

Systemic bronchodilator therapy may or may not be indicated in these cases. If utilized, bronchodilators may worsen ventilation-perfusion inequalities. Thus bronchodilator therapy should be accompanied by supplemental oxygen and the effects should be monitored with serial blood gas measurements and discontinued if hypoxemia worsens. Nebulized or aerosolized bronchodilator therapy may be more judicious, and beneficial effects are evident in some foals with respiratory distress. Examples include albuterol (180-360 μg) or ipratropium bromide (40-80 p.g) or two to four puffs of either, or in combination. Aminophylline and theophylline should not be used because of their narrow therapeutic range. Furosemide (0.5 mg/kg q12h) may be appropriate for its bronchodilator effect and its effect on reducing pulmonary artery pressure, particularly if cor pulmonale develops. It is particularly useful in the management of pulmonary edema. Potential useful therapies in the future may include compounds such as endothelin-1 (ETA) receptor antagonists and inhibitors of fibrosis, such as colchicine.

Prognosis of Interstitial Pneumonia

The prognosis of interstitial pneumonia in horses is uniformly poor to guarded. Affected foals, treated early and aggressively with corticosteroid and antimicrobial therapy, have the best outlook for life. The disease is usually progressive in adults and eventually results in the demise of the horse, although the occasional horse recovers sufficiently to return to previous performance levels. A fair number of adult horses, with continuous intense management, live for a period of time but will be severely compromised, limiting their usefulness.

Exceptions to the poor prognosis may be seen in cases of P. carinii pneumonia in foals if they are treated early and aggressively and in cases of idiopathic interstitial pneumonia in adult horses that are treated early with corticosteroids. A trial of treatment for peracute interstitial disease for 48 hours is warranted and chronic interstitial pneumonia should be treated for a minimum of 2 to 4 weeks before discarding the possibility of recovery.

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Horses

Pleuropneumonia

Thoracic Ultrasonography

Thoracic ultrasonography currently is regarded as the preferred method to diagnose pleuropneumonia in the horse. Although the value of the art of thoracic auscultation and percussion should not be undermined, clinicians managing horses with thoracic disease recognize the limitations of these tools. With the widespread use of thoracic ultrasound, the equine practitioner currently has the ability to determine the presence of pleuropneumonia and the location and the extent of the disease. Although sector scanners are superior (preferably 3.5- to 5.0-MHz transducers), linear probes also can be used to evaluate the thorax in practice.

Thoracic ultrasonography in horses with pleuropneumonia allows the clinician to characterize the pleural fluid and to evaluate the severity of the underlying pulmonary disease. The appearance of the pleural fluid may range from anechoic to hypoechoic, depending on the relative cellularity (). This fluid usually is found in the most ventral portion of the thorax and causes compression of normal healthy lung parenchyma with retraction of the lung toward the pulmonary hilus. The larger the volume of the effusion is, the greater the amount of compression atelectasis and lung retraction that occurs.

The presence of adhesions, pleural thickening, pulmonary necrosis, and compression atelectasis also can be detected. Fibrin has a filmy to filamentous or frondlike appearance and is usually hypoechoic (). Fibrin deposited in layers or in weblike filamentous strands on surfaces of the lung, diaphragm, pericardium, and inner thoracic wall limits pleural fluid drainage. Dimpling of the normally smooth pleural surface results in the appearance of “comettail” artifacts, created by small accumulations of exudate, blood, mucus, or edema fluid. Pulmonary consolidation varies from dimpling of the pleural surface to large, wedge-shaped areas of sonolucent lung ().

Atelectatic lung is sonolucent and appears as a wedge of tissue floating in the pleural fluid. Necrotic lung appears gelatinous and lacks architectural integrity. Peripheral lung abscesses are identified ultrasonographically by their cavitated appearance and the absence of any normal pulmonary structures (vessels or bronchi) detected within. Although detection of a pneumothorax may be easy for the experienced ultrasonagrapher, it is not as easy for the less experienced. The gas-fluid interface can be imaged through simultaneous movement in a dorsal to ventral direction with respiration, the “curtain sign” reproducing the movements of the diaphragm. The dorsal air echo moves ventrally during inspiration, similar to the lowering of a curtain, gradually masking the underlying structures. A pneumothorax without pleural effusion is even more difficult to detect ultrasonographically. Although free bright gas echoes within the pleural fluid can occur after thoracentesis, they are more often seen with anaerobic infections or when sufficient necrosis has occurred in a segment of parenchyma to erode into an airway and form a bronchopleural fistula (). The absence of gas echoes in pleural fluid does not rule out the possibility that anaerobic infection may be present.

Ultrasonography is a valuable diagnostic aid in the evaluation of the pleura, lung, and mediastinum of horses with pleuropneumonia. The detection and further characterization of the above abnormalities improve the clinician’s ability to form a more accurate prognosis. Adhesions can be detected that ultimately may affect the horse’s return to its previous performance level.

Horses with compression atelectasis and a nonfibrinous pleuritis have an excellent prognosis for survival and return to performance. The detection of areas of consolidation, pulmonary necrosis, or abscesses increases the probable treatment and recovery time, and the prognosis for survival decreases as these areas become more extensive. Ultrasonography can be used as a guide to sample or drain the area with a large fluid accumulation or the least loculation. These patients often benefit from progressive scanning to assess response to treatment and the need for drainage.

Pleural Drainage

After selection of an appropriate antimicrobial agent, the next decision to be made is whether to drain the pleural space. Ideally the decision is based on an examination of the pleural fluid. If the pleural fluid is thick pus, drainage using a chest tube should be initiated. If the pleural fluid is not thick pus, but the Gram’s stain is positive and white blood cell (WBC) counts are elevated, pleural drainage is recommended. Another indication for therapeutic thoracocentesis is the relief of respiratory distress secondary to a pleural effusion.

Many options exist for thoracic drainage, including intermittent chest drainage, use of an indwelling chest tube, pleural lavage, pleuroscopy and debridement, open chest drainage/debridement with or without rib resection in the standing horse, open chest drainage/debridement under general anesthesia, and lung resection under general anesthesia. Drainage of a pleural effusion can be accomplished by use of a cannula, indwelling chest tubes, or a thoracostomy. Thoracostomy is reserved for severe abscessation of the pleural space. Thoracocentesis is accomplished easily in the field and may not need to be repeated unless considerable pleural effusion reaccumulates.

Indwelling chest tubes are indicated when continued pleural fluid accumulation makes intermittent thoracocentesis impractical. If properly placed and managed, indwelling chest tubes provide a method for frequent fluid removal and do not exacerbate the underlying pleuropneumonia or increase the production of pleural effusion. The chest entry site and end of the drainage tube must be maintained aseptically. A one-way flutter valve may be attached to allow for continuous drainage without leakage of air into the thorax. If a chest tube is placed aseptically and managed correctly, it can be maintained for several weeks. It should be removed as soon as it is no longer functional. Heparinization of tubing after drainage helps maintain patency. Local cellulitis may occur at the site of entry into the chest but is considered a minor complication. Bilateral pleural fluid accumulation requires bilateral drainage in most horses.

Open drainage or thoracostomy may be considered when tube drainage is inadequate. Open drainage should not begin too early in the disease. An incision is made in the intercostal space exposing the pleural cavity and causing a pneumothorax. If the inflammatory process has fused the visceral and parietal pleura adjacent to the drainage site, a pneumothorax may not develop. The wound is kept open for several weeks while the pleural space is flushed and treated as an open draining abscess.

Pleural Lavage

Pleural lavage may be helpful to dilute fluid and remove fibrin, debris, and necrotic tissue. Lavage apparently is most effective in subacute stages of pleuropneumonia before loculae develop; however, pleural lavage may help break down fibrous adhesions and establish communication between loculae. Care must be exercised that infused fluid communicates with the drainage tube. Lavage involves infusing fluid through a dorsally positioned tube and draining it through a ventrally positioned tube (). In addition, 10 L of sterile, warm lactated Ringer’s solution is infused into each affected hemithorax by gravity flow. After infusion, the ventrally placed chest tube is opened and the lavage fluid is allowed to drain. Pleural lavage probably is contraindicated in horses with bronchopleural communications because it may result in spread of septic debris up the airways. Coughing and drainage of lavage fluid from the nares during infusion suggest the presence of a bronchopleural communication.

Differentiation From Neoplasia

Although pleuropneumonia is the most common cause of pleural effusion in the horse, the second most common cause is neoplasia. Differentiating between the two conditions is a challenge for the equine clinician because similarities exist in the clinical signs and physical examination findings.

Pleuropneumonia effusions are more likely to have abnormal nucleated cell count more than 10,000/μl (usually >20,000/μl) with reater than 70% neutrophils. Bacteria frequently are seen both intra- and extracellularly. A putrid odor may be present.

Neoplastic effusions have variable nucleated cell count. If caused by lymphosarcoma, abnormal lymphocytes may predominate. However, neoplastic cell often are not readily apparent and a definitive diagnosis may be difficult. Rarely do neoplastic effusions have a putrid odor. Bacteria are seen rarely in the cytology preparations.

Once again, use of ultrasonography helps determine if neoplasia is responsible for the effusion. Fibrin most commonly is detected in association with pleuropneumonia but has been detected in horses with thoracic neoplasia. Mediastinal masses associated with neoplasia may be readily visible (). Abnormal solitary masses on the lung surface may be visible in horses with metastatic neoplastic disease.

Comprehensive Management

The primary goals in managing a horse with pleuropneumonia are to stop the underlying bacterial infection, remove the excess inflammatory exudate from the pleural cavity, and provide supportive care. Ideally an etiologic agent is identified from either the tracheobronchial aspirate or pleural fluid and antimicrobial sensitivity determined. Without bacterial culture results, broad-spectrum antibiotics should be used because many horses have mixed infections of both gram-positive and gram-negative and aerobic and anaerobic organisms. Commonly used therapy is penicillin combined with an aminoglycoside such as gentamicin, enrefloxacin, trimethoprim and sulfamethoxazole, or chloramphenicol. Because of the need for long-term therapy, initial intravenous or intramuscular antimicrobials may need to be followed by oral antimicrobials. Preferably the oral antimicrobials are not administered until the horse’s condition is stable and improving because blood levels obtained by this route are not as high as those achieved by use of intramuscular or intravenous administration.

Treatment of anaerobic pleuropneumonia is usually empiric because antimicrobial susceptibility testing of anaerobes is difficult due to their fastidious nutritive and atmospheric requirements. Thus familiarity with antimicrobial susceptibility patterns is helpful in formulating the treatment regimen when an anaerobe is suspected. The majority of anaerobic isolates are sensitive to relatively low concentrations (22,000 IU/kg IV q6h) of aqueous penicillin. Bacteroides fragilis is the only frequently encountered anaerobe that is routinely resistant to penicillin, although other members of the Bacteroides family are known to produce B lactamases and are potentially penicillin-resistant.

Chloramphenicol (50 mg/kg PO q4h) is effective against most aerobes and anaerobes that cause equine pleuropneumonia. However, because of human health concerns the availability of chloramphenicol may decrease. Metronidazole has in vitro activity against a variety of obligate anaerobes including B. fragilis. Pharmacokinetic studies indicate a dose of 15 mg/kg intravenously or orally four times a day is necessary to maintain adequate serum levels. Oral administration rapidly results in adequate serum levels and thus is an acceptable route of administration for horses with pleuropneumonia. Metronidazole is not effective against aerobes and therefore always should be used in combination therapy at a dose of 15 mg/kg every 6 to 8 hours. Side effects of metronidazole include loss of appetite and lethargy; use of the drug should be halted when these signs are observed. Aminoglycosides and enrofloxacin should not be considered for the treatment of pleuropneumonia caused by an anaerobe unless these drugs are used in combination therapy with penicillin.

Ancillary Treatment

Antiinflammatory agents help reduce pain and may decrease the production of pleural fluid. This in turn may encourage the horse to eat and maintain body weight. Flunixin meglumine (500 mg ql2-24h) or phenylbutazone (1-2 g q12h) is commonly used for this purpose. In this author’s opinion, corticosteroids are contraindicated for the treatment of bacterial pleuropneumonia. Rest and the provision of an adequate diet are important components of the treatment of pleuropneumonia. Because the disease course and period of treatment are usually prolonged, attempts should be made to encourage eating. Intravenous fluids may be indicated in the acute stages of the disease to treat dehydration resulting from anorexia and third-space losses into the thorax.

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Horses

Permanent Tracheostomy in Standing Horses

Diseases of the upper airway such as laryngeal hemiplegia, arytenoid chondritis, subepiglottic cysts, aryepiglottic fold entrapment, and dorsal displacement of the soft palate are commonly encountered in horses. In all of these conditions some abnormality of the upper airway compromises the cross-sectional area of the airway and causes decreased airflow; the condition usually becomes clinically significant only at exercise. In the majority of these cases, surgical correction specifically addresses the area of compromise and corrects the abnormality.

Certain conditions exist, however, in which the lesion causes such severe stenosis of the upper airway that surgical correction of the lesion is met with a guarded or poor long-term prognosis. In this author’s experience and based on literature review, the most common conditions in which less invasive procedures have failed are related to the problem of nasopharyngeal cicatrix. In this syndrome, a circular web of tissue forms in the pharynx, first ventrally over the floor of the pharynx and then dorsally, in which position it extends above the pharyngeal openings of the guttural pouches. Arytenoid chondritis is commonly associated with this generalized inflammatory process. Resection of the diseased cartilage does not seem to be curative because the generalized inflammatory process continues with the subsequent pharyngeal/laryngeal swelling that leads to obstruction of the airway. In these cases, permanent tracheostomy can provide an effective alternative approach by bypassing the obstruction. Other indications for a permanent tracheostomy are neoplasia of the upper airway and severe deformity of the nasal passages.

Surgical Technique

Although permanent tracheostomy can be performed with the horse under general anesthesia, the technique described here can be readily performed in the standing horse. This provides some advantages because the surgical structures are in a more normal anatomic orientation and create less tension on the tracheostomy closure during the healing period. This position also avoids complications associated with general anesthesia and recovery and reduces the expense of the procedure.

Perioperative antibiotics (procaine penicillin G, 20,000 IU/kg q12h, IM) and antiinflammatories (flunixin meglumine, 1.1 mg/kg IV) should be administered. The horse is restrained in the stocks and cross-tied so that it is positioned forward in the stocks with its head extended in front of the side poles of the stocks. With this restraint, the surgeon has easy access to the surgical area. Maintenance of this position is easier if the horse’s head is suspended from a bar that extends from the top of the stocks over the head. The head is suspended by means of the halter that is placed upside down so that the throat-latch strap is over the horse’s forehead (between the eyes and ears) and not under the throat adjacent to the surgical site. Padding should be placed between the halter and the mandible to prevent facial nerve paralysis. Placement of the horse’s head in a stand similar to a crutch may also help in maintaining the head and neck in an extended position. Sedation and analgesia is provided by administration of detomidine (0.02 mg/kg, half administered IV and half IM) and butorphanol (0.011 to 0.022 mg/kg IV).

The incision is positioned over the second to sixth tracheal rings. Local anesthesia is infiltrated subcutaneously in an inverted U pattern dorsal and lateral to the second through sixth tracheal rings. Starting approximately 3 cm distal to the cricoid cartilage and centered over midline, the surgeon removes a 3-cm wide x 6-cm long rectangular section of skin. The surgeon then continues the incision on midline, separating the paired sternothyrohyoideus muscles to expose the tracheal rings. Dissection is performed laterally around the abaxial borders of the paired sternothyrohyoideus muscle. The muscle bellies are isolated and clamped (Ferguson Angiotribe Forceps; Miltex, Lake Success, N.Y.) at their proximal and distal exposure in the incision. After clamping for several minutes to crush the vessels, the muscle bellies are transected. This author also recommends removal of a section of the omohyoid muscle in a similar fashion. The fascia covering the tracheal rings is carefully removed. A ventral midline incision and two paramedian incisions, approximately 15 mm on either side of the midline incision, are made through the tracheal ring cartilage without penetrating the tracheal mucosa. The tracheal cartilage segments are carefully dissected free from the tracheal submucosa, leaving the submucosa and mucosa intact. Although this may appear very difficult, the mucosa is thick and separates easily from the rings with patient dissection.

Most commonly a total of five tracheal rings (two through six) are removed although removal of four rings is often adequate. To alleviate dead space, subcutaneous tissue is sutured to the tracheal fascia with 0-polydioxane (PDS; Ethicon Inc, Somerville, NJ.) with use of a simple interrupted pattern. In some horses this author inserts a 23-gauge, 2.5-cm needle into the lumen of the trachea and injects 30 ml of 25% lidocaine HCl proximal to the incision to desensitize the tracheal mucosa. The tracheal mucosa is incised in what has been described as a double Y pattern. In this pattern, a central midline incision is made that ends approximately one tracheal ring width before the rostral and caudal ends of exposed tracheal mucosa. The midline incision is extended as a V with each leg connecting to the corners of one end of the exposed rectangular section of tracheal mucosa. In this way, a double Y pattern is formed. The surgeon sutures the tracheal mucosa and submucosa to the skin with simple interrupted sutures of 0-polydioxone, starting at the ends and then suturing along the lateral borders.

Permanent Tracheostomy in Standing Horses: Aftercare

Because the proximal trachea is not a sterile environment, antibiotics should be administered for 5 to 7 days postoperatively. Nonsteroidal antiinflammatory drugs should be continued for 5 to 7 days depending on the amount of postoperative swelling. The stoma should be cleaned once or twice daily until the sutures are removed 10 to 14 days after surgery. The stoma needs to be cleaned daily for the first month after surgery, but usually by 1 to 2 months postoperatively the discharge will decrease and make daily cleaning unnecessary. In the majority of this author’s long-term postoperative cases, cleaning has been necessary only once or twice a week.

In this author’s experience, postoperative swelling with or without partial dehiscence is the most commonly encountered complication. Incisions that develop partial dehiscence can heal satisfactorily by second intention. In some cases the areas of partial dehiscence have had to be surgically repaired, a method that usually involves removing more of the adjacent muscle and resuturing the mucosa and submucosa to the skin. In a small percentage of cases that had insufficient stoma size repairs were made by removing sections of the omohyoid muscle. Because of this experience, this author now routinely removes a portion of the omohyoid when performing a tracheostomy.

Permanent Tracheostomy in Standing Horses: Prognosis

In this author’s experience the long-term prognosis after tracheostomy is good, and more than 90% of owners say that they are pleased with the outcome. Tracheostomy has been performed on many broodmares without causing problems during foaling, although close observation of the mare around the foaling period is still recommended. In some horses the tracheostomies were performed more than 10 years ago and the stoma is still patent and causes no problems. This procedure does not prevent the horse from being used for athletic purposes; some of the aforementioned horses are used for pleasure riding and some used as Western performance horses. Although the tracheostomy bypasses a component of the pulmonary defense mechanism that acts to moderate temperature and humidity and filter inspired air, these horses have not appeared to be predisposed to airway infections. Approximately one fourth cough occasionally during exercise, most likely because of irritation of the trachea from dust particles. Consequently maintenance of the horses in an environment that is as dust-free as possible is recommended.

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Horses

Postanesthetic Upper Respiratory Tract Obstruction

Upper respiratory tract () obstruction can occur in horses recovering from general anesthesia after various surgical procedures. Postanesthetic upper respiratory tract obstruction most often results from nasal edema and/or congestion and is usually mild. Other causes include arytenoid chondritis, dorsal displacement of the soft palate, and bilateral arytenoid cartilage paralysis. Bilateral arytenoid cartilage paralysis is relatively uncommon; however, it can result in severe upper respiratory tract obstruction with the horse becoming distressed, uncontrollable, and difficult to treat. The condition may rapidly become fatal, thus postanesthetic upper respiratory tract obstruction can be a serious complication after general anesthesia and surgery.

Etiology of Postanesthetic Upper Respiratory Tract Obstruction

Nasal Edema

Nasal edema and/or congestion is most often the result of venous congestion associated with a dependent head position during a prolonged anesthesia. Horses positioned in dorsal recumbency are thought to be more prone to nasal edema than horses in lateral recumbency. Nasal and pharyngeal edema may also result from trauma during endotracheal intubation that causes local inflammation and swelling.

Dorsal Displacement of the Soft Palate

Causes of dorsal displacement of the soft palate after ex-tubation are unknown. The condition is most likely a normal consequence of orotracheal intubation and of administration of sedative and anesthetic drugs that alter upper respiratory tract neuromuscular function. If dorsal displacement persists, it is most likely the result of an underlying upper respiratory tract problem or of inflammation in the pharynx secondary to intubation.

Arytenoid Chondritis

Arytenoid chondritis is an uncommon cause of postanesthetic upper respiratory tract obstruction but can be a longer-term consequence of traumatic intubation. Although this condition will not lead to obstruction in the same anesthetic period, it may at a later time if it is not recognized. Furthermore, the presence of an abnormal arytenoid will compromise the airway and can potentiate the possibility of an obstructive crisis.

Bilateral Laryngeal Paralysis

The etiology of postanesthetic bilateral laryngeal paralysis is unknown. Proposed etiologies include inflammation and edema of the larynx and neuromuscular failure. Physical trauma from endotracheal intubation or chemical irritation from residue after endotracheal tube cleaning may result in arytenoid chondritis, laryngeal dysfunction, and laryngeal inflammation and swelling. Laryngeal edema from venous congestion associated with a dependent head position during a prolonged anesthesia may cause swelling and failure of the arytenoid cartilages to adequately adduct. Causes of neuromuscular failure that lead to bilateral arytenoid cartilage paralysis include trauma to the cervical region or jugular vein; compression of the recurrent laryngeal nerve between the endotracheal tube or cuff and noncompliant neck structures; damage to the recurrent laryngeal nerve from intraoperative hypoxia, ischemia, or hypotension; and overextension of the neck when the horse is positioned in dorsal recumbency that causes damage to the recurrent laryngeal nerve as a result of compression of its blood supply.

α2-Adrenergic agonists have been shown to increase laryngeal asynchrony and increase upper airway resistance in horses. The muscle relaxant effects of xylazine are thought to decrease the tone of the supporting airway muscles, which in combination with low head carriage may cause an increase in airway resistance. The muscle relaxant effects of xylazine may have worn off at the time the horse has recovered from anesthesia; however, one study showed that upper airway resistance increased for 30 to 40 minutes after xylazine administration and then slowly returned to normal. Impaired laryngeal function associated with xylazine administration in combination with excitement associated with recovery from anesthesia and extubation may lead to dynamic collapse of the upper respiratory tract and result in the clinical signs described. Xylazine is a commonly used preanesthetic drug; therefore although it is unlikely to be the sole cause of the upper respiratory tract obstruction, it may be a contributing factor.

Underlying upper respiratory tract disease such as laryngeal hemiplegia may also predispose horses to severe postanesthetic obstruction. A few reports exist in the literature of severe postanesthetic upper respiratory tract obstruction in horses associated with laryngeal dysfunction. In two previous reports, bilateral arytenoid cartilage paralysis was associated with surgery in the head and neck region, and the horses recovered after establishment of a patent airway. These authors have recently seen several postanesthetic upper respiratory tract obstructions in horses that have undergone surgery for a variety of reasons including arthroscopy, tarsal arthrodesis, exploratory celiotomy, ovariohysterectomy, mastectomy, and prosthetic laryngoplasty/ventriculectomy. In addition to having undergone prosthetic laryngoplasty, some of these horses had a history of laryngeal hemiplegia before surgery. This fact suggests that preexisting disease may predispose to this condition. Postanesthetic upper respiratory tract obstruction in the horses at these authors’ hospital is often associated with excitement or exertion, including standing after anesthesia and vocalization. The cause of severe obstruction therefore could be laryngospasm or dynamic adduction of both paretic arytenoid cartilages into the airway during inspiration.

In the horses at these authors’ hospital, no association exists between difficult endotracheal intubation and upper respiratory tract obstruction. In horses that developed obstruction the duration of anesthesia was 90 to 240 minutes, and horses had mild-to-moderate hypotension, hypoventilation, and hypoxemia. These authors clean their endotracheal tubes with chlorhexidine gluconate between uses. If the tubes are not rinsed adequately, mucosal irritation from residual chlorhexidine gluconate could conceivably cause upper respiratory tract irritation and lead to obstruction. Most important, however, all these horses were positioned in dorsal recumbency for at least some of the time they were under anesthesia. The horses are positioned on a waterbed from the withers caudad. This position results in hyperextension of the neck and a dependent head position, both of which may predispose to postanesthetic bilateral arytenoid paralysis.

Negative-Pressure Pulmonary Edema

Pulmonary edema can result from upper respiratory tract obstruction and has been referred to as negative-pressure pulmonary edema because the pulmonary edema occurs secondary to strong inspiratory efforts against a closed airway. In humans vigorous inspiratory efforts against a closed glottis may create a negative pressure of as low as -300 mm Hg that, obeying Starling’s laws of fluid dynamics, fluid moves from the intravascular space into the interstitium and alveoli.

Clinical Signs

Although upper respiratory tract obstruction usually occurs immediately after extubation, severe obstruction associated with bilateral arytenoid paralysis may occur within 24 to 72 hours of recovery from anesthesia. The most obvious clinical sign is upper respiratory tract dyspnea. Horses with nasal edema have a loud inspiratory snoring noise, whereas horses with dorsal displacement of the soft palate have an inspiratory and expiratory snoring noise associated with fluttering of the soft palate. Horses with severe upper respiratory tract obstruction from bilateral laryngeal paralysis have a loud, high-pitched, inspiratory stri-dor associated with exaggerated inspiratory efforts.

Treatment of Postanesthetic Upper Respiratory Tract Obstruction

Nasal Edema

The most common type of upper respiratory tract obstruction is nasal edema, which often resolves rapidly without treatment. If obstruction is severe, it is critical to create a patent airway. The horse should be reintubated with a nasotracheal or orotracheal tube or 30-cm tubing placed in the nostrils to bypass the obstruction. Phenylephrine intranasal spray (5-10 mg in 10 ml water) or furosemide (1 mg/kg) may be used to reduce the nasal edema. Edema can be prevented by atraumatic intubation, reducing surgery time, and keeping the horse’s head elevated during anesthesia and surgery.

Dorsal Displacement of the Soft Palate

Dorsal displacement of the soft palate usually resolves spontaneously when the horse swallows, however, it may be corrected through induction of swallowing by gentle manipulation of the larynx or by insertion of a nasogastric tube into the pharynx.

Bilateral Laryngeal Paralysis

Severe obstruction often develops when the horse stands after being extubated. Emergency treatment is required because the horse will rapidly become severely hypoxic, develop cardiovascular collapse, and die. Horses are often difficult to treat because obstruction may not be noticed until the horse is severely hypoxic and uncontrollable. Treatment is then delayed until the horse collapses from hypoxia, however, emergency reintubation or tracheostomy is often too late.

Immediate treatment consists of rapid reintubation or tracheostomy. Horses may be reintubated with a nasotracheal tube (14-22 mm) or an orotracheal tube (20-26 mm). The clinician performs a tracheostomy by clipping, preparing, and blocking the ventral cervical region (if time permits), making a 8-cm vertical incision on midline at the junction of the upper and middle thirds of the neck, bluntly separating the sternothyrohyoideus muscles, and then making a transverse incision between the tracheal rings. These authors recommend having a kit available with a tracheostomy tube and drugs for reinduction of anesthesia (xylazine, 1.1 mg/kg; ketamine, 2.2 mg/kg; or a paralytic agent such as succinylcholine, 330 μg/kg IM). Horses should be treated with insufflation of oxygen immediately after establishment of an airway.

Prevention of upper respiratory tract obstruction after anesthesia requires treatment of hypotension, hypoxemia, and hypoventilation, avoidance hyperextension of the neck when horses are positioned in dorsal recumbency, and thorough rinsing of endotracheal tubes. These authors recover horses with the oral endotracheal tube in place, and following extubation closely monitor air movement.

If the horse has bilateral laryngeal paralysis, it may be necessary to establish a tracheostomy while the horse is treated aggressively with antiinflammatory treatment. Recovery should occur within days.

Negative-Pressure Pulmonary Edema

Previous reports have described successful treatment of negative-pressure pulmonary edema, however, treatment may fail if a delay occurs between obstruction and treatment or if an unknown underlying disease is present. Treatment of negative-pressure pulmonary edema consists of administration of oxygen through nasal insufflation (10-15 L/min for an adult horse), a diuretic (furosemide, lmg/kg IV, and mannitol, 0.5-1.0 g/kg IV), antiinflammatory agents (flunixin meglumine, 1.1 mg/kg; dexamethasone, 0.1-0.3 mg/kg; dimethyl sulfoxide [DMSO]; lg/kg), and the positive inotrope epinephrine (2-5 μg/kg). Fluid therapy with polyionic isotonic fluids and electrolytes should be administered, however, overhydration of horses with pulmonary edema must be avoided.

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Treatment of Vasculitis

Treatment of purpura hemorrhagica and similar idiopathic vasculitides consists of the following: (1) removing the antigenic stimulus; (2) suppressing the immune response; (3) reducing vessel wall inflammation; and (4) providing supportive care. Any drugs given when the clinical signs occurred should be discontinued, or, if continued medication is necessary, an alternate drug should be chosen from a chemically unrelated class. A thorough examination should be performed to identify a primary disease process. Any bacterial pathogens should be cultured and an in vitro sensitivity performed. Because most cases of purpura hemorrhagica are a sequela of Streptococcus equi infection, penicillin (procaine penicillin G 22,000-44,000 U/kg IM q12h or sodium or potassium penicillin 22,000-44,000 U/kg IV q6h) should be administered for a minimum of 2 weeks unless specifically contraindicated. Any accessible abscess should be drained. If gram-negative bacteria are suspected or isolated, additional appropriate antimicrobial therapy should be used. Antimicrobial therapy is also indicated to limit or prevent secondary septic complications such as cellulitis, tenosynovitis, arthritis, pneumonia, and thrombophlebitis.

Systemic glucocorticoids are warranted because purpura hemorrhagica and other undefined vasculitides are most likely immune-mediated. In addition, systemic glucocorticoids reduce inflammation of the affected vessel walls and subsequent edema formation. Dexamethasone (0.05-0.2 mg/kg IM or IV q24h) or prednisolone (0.5-1.0 mg/kg IM or IV q24h) may be used; however, clinical experience indicates that dexamethasone is more effective during initial therapy. The minimum dose that provides a decrease in clinical signs should be used. After substantial reduction and stabilization of clinical signs, the dose of glucocorticoids may be decreased by 10% per day over 10 to 21 days. When the dose of dexamethasone is 0.01 to 0.04 mg/kg per day, it may be given orally; alternatively, prednisolone may be substituted at ten times the dexamethasone dose. The bioavailability of oral prednisolone is 50%; thus an effective parenteral dose administered orally may result in relapse of clinical signs. Prednisone is poorly absorbed from the gastrointestinal tract and is not detectable in the blood of most horses after oral administration; thus its use is not recommended. Hydrotherapy, application of pressure bandages, and hand-walking should be used to decrease or prevent edema. Furosemide (1 mg/kg IV q12h) may help reduce edema in severe cases. A tracheostomy may be indicated if respiratory stridor is present from edema of the nasal passages, pharynx, and/or larynx. Dysphagic horses should be supported with intravenous or nasogastric administration of fluids. Nutritional support may be necessary in horses with prolonged dysphagia. Nonsteroidal antiinflammatory drugs (flunixin meglumine 1.1 mg/kg IV, IM or PO q12h or phenylbutazone 2.2-4.4 mg/kg IV or PO q12h) are indicated to provide analgesia in horses with lameness, colic, myalgia, or other painful conditions. NSAIDs may also help reduce the inflammation in affected vessel walls.

Horses with equine viral arteritis do not require specific therapy because the majority of cases recover uneventfully. Glucocorticoids are contraindicated because vessel wall damage results from direct viral injury. Occasionally horses with severe clinical signs of lower respiratory disease will need antimicrobial therapy to prevent or treat secondary bacterial pneumonia. Horses with EIA are infected for life. Glucocorticoids are contraindicated because they may result in increased viral replication and occurrence of clinical disease. Horses with equine ehrlichiosis may benefit from glucocorticoid therapy; however, they should be treated with oxytetracycline to eliminate the organism (see: “Equine Monocytic Ehrlichiosis” and: “Hemolytic Anemia”). Horses with photoactivated vasculitis should be stabled during daylight hours to prevent any further exposure to sunlight. The vascular inflammation should be treated with systemic glucocorticoids in a regimen similar to that for purpura hemorrhagica. Topical applications of glucocorticoids with or without antibiotics are not effective. Irritating topical solutions should not be used.

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Acquired Coagulation Disorders

Disseminated Intravascular Coagulation

Disseminated intravascular coagulation () is the most common hemostatic dysfunction in the horse. disseminated intravascular coagulation is an acquired process in which activation of coagulation causes widespread fibrin deposition in the microcirculation resulting in ischemic damage to tissues. Hemorrhagic diathesis occurs as a result of consumption of procoagulants or hyperactivity of fibrinolysis. In normal coagulation, thrombin activates the conversion of plasma soluble fibrinogen to the insoluble fibrin, which forms a clot. Simultaneously, the fibrinolytic system is activated to prevent tissue ischemia that would occur from persistent fibrin clots. The fibrinolytic protein that is primarily responsible for limiting fibrin clot formation and providing a mechanism for clot removal is plasmin. Antithrombin III and protein C also minimize clot formation by inhibiting the actions of thrombin and as well as some of the other clotting factors. In disseminated intravascular coagulation, antithrombin III and protein C become depleted as a result of overzealous activation of coagulation. This results in excessive, unchecked thrombin and clot formation, which in turn activates plasmin. FDPs are formed when plasmin degrades fibrin. As the FDPs begin to accumulate in the circulation, they contribute to the coagulopathy by inhibiting thrombin activity and by causing platelet dysfunction. The end result is the dynamic combination of disseminated thrombosis at the same time that clotting factor consumption and fibrinolysis potentiate bleeding.

Disseminated intravascular coagulation is not a primary disease; it occurs in conjunction with diseases that generate excessive procoagulant activity in the blood. Diseases related to the gastrointestinal system (e.g., strangulating obstruction, colitis, enteritis), sepsis, renal disease, hemolytic anemia, and neoplasia are the most common primary diseases associated with disseminated intravascular coagulation. In one study, 96% of the horses that developed disseminated intravascular coagulation over a 5-year period were diagnosed with colic that required surgical intervention. Horses with devitalized intestine that required resection and anastomosis were more likely to develop disseminated intravascular coagulation than those horses in which resection and anastomosis was not required. Because endotoxin is a prominent feature of ischemic or inflammatory disease of the equine gastrointestinal tract, it is a logical conclusion that endotoxemia is the underlying pathophysiologic event that most commonly triggers disseminated intravascular coagulation. Endotoxin can initiate disseminated intravascular coagulation by several mechanisms: (1) direct damage to the endothelium, thereby releasing tissue factor; (2) induction of tissue factor expression and cytokine synthesis by mononuclear phagocytes; (3) direct activation of factor XII; (4) stimulation of thromboxane A2 synthesis by platelets which promotes irreversible platelet aggregation; and (5) inhibition of fibrinolysis by increasing production of plasminogen activator inhibitor.

Clinical Signs

Clinical signs of disseminated intravascular coagulation range from mild thrombosis and ischemic organ failure to petechiae and hemorrhage. In contrast to humans, frank hemorrhage associated with disseminated intravascular coagulation is rare. Petechial or ecchymotic hemorrhages of the mucous membranes or sclerae, epistaxis, hyphema, and melena can occur. Hypoperfusion and microvascular thrombosis lead to focal or widespread tissue damage and culminates in colic; laminitis; and signs of renal, pulmonary, and cerebral disease. Peripheral veins are susceptible to spontaneous thrombosis as well as increased thrombus formation after catheterization or simple venipuncture. Clinical signs of the primary underlying disease may overshadow the initial signs of disseminated intravascular coagulation.

Diagnosis

A single test cannot confirm disseminated intravascular coagulation. The presence of clinical signs — thrombocytopenia, prolonged APTT and PT, and an increase in FDP concentration (>40 fig/ml) — is consistent with disseminated intravascular coagulation. In the early stages of disseminated intravascular coagulation, FDPs may not be increased. Monitoring changes over time can help decipher difficult cases, as thrombocytopenia and prolongation of the PT are frequently the only abnormalities initially detected. Hypofibrinogenemia is an uncommon finding in the horse; in fact, fibrinogen concentration may be increased, depending on the duration of the underlying primary disease. Reduced antithrombin III activity (<80% normal) also supports a diagnosis of disseminated intravascular coagulation.

Treatment and Prognosis

Determining the correct therapy for disseminated intravascular coagulation is difficult and controversial. Identification and treatment of the underlying disease process is paramount. Intravenous fluid therapy is necessary to maintain tissue perfusion and combat shock. If a septic process is present, antimicrobials are indicated. If a strangulating intestinal obstruction is present, immediate surgical correction is warranted. Minimizing the effects of endotoxemia may attenuate the disease process (see Chapter 3.7: “Endotoxemia”). Flunixin meglumine (0.25 mg/kg IV q8h) will mitigate the detrimental effects of eicosanoids. Corticosteroids are contraindicated because they potentiate the vasoconstrictive effect of catecholamines and reduce the activity of the mononuclear phagocyte system, which exacerbates coagulopathy by enabling FDPs to accumulate.

Fresh plasma therapy (15-30 ml/kg of body weight) is indicated with severe hemorrhage. It should be noted that administration of plasma could exacerbate thrombosis by supplying more clotting factors to “fuel the fire.” Fresh whole blood can be given if anemia is present from blood loss. Although its use remains controversial, administration of heparin (20 to 100 U/kg SQ q8-12h) in conjunction with fresh plasma may minimize clot formation by potentiating the anticoagulative effects of antithrombin III. Thus if heparin therapy is to be used, adequate antithrombin III must be present. Heparin can cause thrombocytopenia, hemorrhage, and reversible erythrocyte agglutination. If heparin is used, the packed cell volume should be closely monitored for a sudden decline. Low-molecular-weight heparin (Fragmin, Kabi Pharmacia AB; Stockholm, Sweden; 50 U/kg SQ ql2h) does not cause agglutination of equine erythrocytes, but its use may be cost-prohibitive. The prognosis for disseminated intravascular coagulation depends on the severity of the underlying disease and the response to therapy. In general, the prognosis is guarded to poor. In humans, the mortality rate is 96% when the antithrombin III activity falls below 60%.

Warfarin and Sweet Clover Toxicosis

Horses may develop hemorrhagic diathesis after consuming warfarin for therapeutic reasons, rodenticides, or moldy sweet clover (Melilotus spp.). Warfarin has been used for treatment of thrombophlebitis and navicular disease. Combination of warfarin with other protein-bound drugs, such as phenylbutazone, results in toxic accumulation in the plasma. Sweet clover hay or silage that is improperly cured can contain dicumarol. The toxin is not present in the living plant. The pathogeneses of warfarin and sweet clover toxicosis are identical. Dicumarol and warfarin competitively inhibit vitamin K, which is necessary for the production of clotting factors II, VII, IX, X.

The clinical signs of warfarin or dicumarol toxicosis include hematomas, hematuria, epistaxis, and ecchymoses of the mucous membranes. Absence of petechial hemorrhages can distinguish warfarin and dicumarol toxicity from disseminated intravascular coagulation. The diagnosis is made based on history of exposure and laboratory data. Clinical pathology reflects prolonged PT first because the plasma half-life of factor VII is shorter than the other clotting factors. The APTT becomes prolonged, but the platelet count remains normal.

Treatment for warfarin toxicity may only require discontinuation of the drug. If accidental exposure to rodenticides or dicumarol occurs, treatment with vitamin K, (0.5 to 1 mg/kg of body weight SQ q6h) 3 to 5 days is recommended. Therapy should be guided by measuring PT. Vitamin K3 causes acute renal failure and should not be given to horses. In an acute crisis, plasma or a whole blood transfusion may be indicated.

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Treatment of RFM

Although many mares with RFM do not become clinically ill, early prophylactic intervention is widely practiced because the complications associated with RFM may be severe and potentially life threatening. Many farm managers and horse owners with a veterinary client-patient relationship may be instructed to begin intramuscular (IM) injections of oxytocin 2 to 4 hours postpartum if the fetal membranes have not been passed. The membranes should be tied up above the hocks to prevent soiling and tearing. Tying a weight (e.g., a brick) to the membranes is not recommended because it may predispose the mare to development of a uterine horn intussusception. Injections of oxytocin should be given every hour for at least 6 treatments. The half-life of oxytocin in the mare is brief (12 min).

The initial starting dose of oxytocin should be on the low side (10-20IU/500 kg) because sensitivity to oxytocin varies widely. The dose of oxytocin can then be tailored to each individual mare. A positive response will result in passage of uterine fluid from the vagina. Mares should be monitored following injection because any obvious cramping will begin within 10 minutes of IM injection. If a 10- to 20-IU oxytocin treatment does not result in an outward manifestation of discomfort by the mare, such as sweating and restlessness, then the dose can be increased in 10- to 20-IU increments until an effect is noticed. The dose should only be high enough to elicit mild colic signs. Mares with uterine inertia because of dystocia may be initially very resistant to the effect of oxytocin and may become more sensitive in the subsequent hours. If cramping and rolling result then the dose should be reduced. Some mares become inattentive mothers during the time when they are distracted by RFM or uncomfortable from the oxytocin-induced cramping. Thus the foal should be kept in a safe place when the mare is in pain. Nursing should be encouraged to stimulate the natural release of oxytocin associated with milk letdown.

If the mare fails to respond to six oxytocin injections or if she is clinically ill, a thorough veterinary examination is indicated. One option is to start an intravenous (IV) drip of oxytocin at 0.1 IU/ml of saline (i.e., 100 IU oxytocin per 1 L saline). The IV flow rate should be set so that the mare has visible signs of contractions every S to 10 minutes. The oxytocin drip treatment protocol will, in effect, revert the mare back into labor for about 1 hour.

The technique described by Burns and colleagues () works best when the membranes are fresh. Some clinicians perform the procedure prophylacti-cally after a dystocia to reduce the likelihood of membrane retention. The clinician should wear waterproof clothing and a sterile surgical glove over a clean rectal sleeve. The perineum of the mare and external portion of the membranes are washed thoroughly. The opening at the cervical star, which leads into the allantoic cavity, is identified. A clean large-bore stomach tube is introduced, and the membranes are gathered around the tube. In addition, 4 L or more of a warm 1% povidone iodine solution is pumped or gravity fed into the chorioallantois until the fluid overflows. The tube is withdrawn as the RFM are tied shut with umbilical tape. Oxytocin may then be administered so that the uterus contracts against the distended membranes. This technique distends the endometrial crypts and often permits release of the microcotyledons. If the procedure is unsuccessful then it may be repeated several hours later. However, the retained membranes soon become autolytic and tend to tear as soon as distention starts.

If partial retention of the membranes is diagnosed, or if the membranes are badly torn, the uterus may be distended with 1% povidone iodine solution as described previously. The fluid distention and uterine contractions may help loosen the membranes. If the piece of membrane can be reached, it may be gently teased off the en-dometrium and removed. However, if the membrane tag is firmly adhered then continued traction is contraindicated. Once or twice daily flushing and the process of au-tolysis will eventually loosen the membranes. This procedure also may be carefully performed in mares that retain the membranes after a cesarean section. However, it is important to use a lower volume of infusate so that the uterine closure and fibrin seal are not disrupted.

Toxemic mares that are clinically ill and are passing a fetid uterine discharge may require systemic support with IV fluids, frequent IV treatments with oxytocin, and twice daily high-volume uterine lavage. Gentle manual removal of the fetid membranes may be necessary in these mares. Back and forth uterine lavage is performed with a clean stomach tube, bilge, or stomach pump. A dilute (1%) povidone iodine solution or sterile fluids are used to remove bacteria and inflammatory debris from the uterus. The clinician should hold the end of the tube cupped in the hand within the uterine cavity to prevent the tube from forcefully sucking against the wall when the fluid is being siphoned back. During the first few lavage procedures, persistence and patience in obtaining a clean return from the uterus is often rewarded with rapid clinical improvement and uterine involution. Lavage should be repeated once or twice daily until all debris is removed, the lavage is clear, and the uterus is well involuted.

Prophylactic administration of antibiotic and antiinflammatory medication is often prescribed early in the course of RFM in an attempt to prevent complications. Common antimicrobial choices are trimethoprim sulfa (30 mg/kg, q24h PO), or procaine penicillin G (22,000 IU/kg ql2h IM) for a minimum of 3 to 5 days. If the mare is systemically ill then broad-spectrum medications such as penicillin-aminoglycoside combinations are recommended. The formulations or derivatives of penicillin include the following: procaine penicillin (22,000 IU/kg ql2h IM), sodium and potassium penicillin (22,000 IU/kg q6h IV), ampicillin (50 mg/kg q8h IV), or ticarcillin (44 mg/kg q8h IM) for resistant cases. Aminoglycosides such as gentamicin (6 mg/kg q24h IM or IV) or amikacin (6.6 mg/kg ql2h IV or IM) are used for mixed and gram-negative infections or resistant cases. Appropriate antibiotic use is confirmed by uterine culture and sensitivity results.

The mostly commonly used antiinflammatory medication for endotoxemic mares is flunixin meglumine, 1.1 mg/kg IV. In milder cases, flunixin meglumine (0.25-0.5 mg/kg q8h IV), ketoprofen (2 mg/kg ql2h IV), vedaprofen (2 mg/kg ql2h PO), or phenylbutazone (4 mg/kg IV or PO) are used. Hyperimmune plasma is administered if it is available.

Laminitis in mares with RFM is a serious complication. Lateral radiographs of the distal phalanx will help establish the degree of rotation, and the prognosis. Symptomatic care such as hosing the hooves with cold water, or application of foam pads or special shoes to the hooves can provide extra support and promote comfort. Phenylbutazone at 2 g every 24 hours by mouth is sometimes used prophylactically.

Mares with lactation failure should be treated with domperidone at 1.1 mg/kg orally every 12 hours to encourage lactation.

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Algorithm For Emergency Treatment Of Hemorrhage In The Broodmare

A simplified, step-by-step, sample flow chart for hemorrhage treatment is outlined below. The clinician should keep in mind that this outline describes an attempt to treat what should be a surgical problem, medically. One can only surmise at the nature of the internal insult. Periodic evaluation of the mare without quantification of the severity of the internal blood loss and the benefit of blood pressure measurements makes this a very challenging situation.

1. Obtain initial vital signs.

2. If internal bleeding is suspected and the mare is hypovolemic, insert a large-bore (12- to 14-gauge) IV catheter into the left, or most easily accessible, jugular vein. It may be prudent to catheterize both jugular veins, as these mares change positions frequently and because violent head movement may dislodge a catheter.

3. Administer 2 to 3 L of warmed hypertonic saline. Warmed saline has been shown not only to provide plasma expansion, but also to exert some cytoprotective properties by attenuating harmful humoral cascades.

4. Follow hypertonic saline with 2 to 3 L of a warmed polyionic crystalloid such as Normosol-R or Plamalyte. These solutions contain readily available buffers such as acetate and gluconate that do not need to be converted by the liver. They are available in rigid plastic containers that can be pressurized by a hand pump. This small amount of crystalloid furnished will often calm and stabilize a mare. The goal is to volume expand just enough to deliver oxygen and nutrients to cells, yet not to elevate blood pressure so that it will dislodge what hopefully is a growing clot at the site of injury. The clinician should not become overzealous in fluid administration without reevaluating vital parameters.

5. Try to make the mare’s environment conducive to clot formation (i.e., lessen noise and distractions, create warmth with heat lamps and blankets if it is severely cold), provide water to drink at regular intervals and in appropriate amounts, and if the mare is lying down, let her continue to do so because this may provide some pressure on internal organs and help to stem hemorrhage.

6. Attempt to characterize the site and magnitude of blood loss to better assess the time and expense that may be involved in a continued resuscitative effort. If fluid is found on transabdominal ultrasound, abdominocentesis and fluid analysis is strongly advised.

7. After the initial crystalloids, 3 to 4 L of plasma are highly recommended because they will provide proteins and clotting factors. If owners are willing to spend money and the mare is valuable, plasma is probably the most important “medication” to give. This colloid can be kept in the freezer at home so that it is convenient to take to an emergency, or have it picked up by a farm employee. Thawed plasma can be kept in a refrigerator or cooler for as long as 7 days or more.

8. Reevaluate vital signs and determine if more fluids should be given. A stall-side chart to jot down the course of medications and the amounts administered is highly recommended.

9. Consider taking a peripheral blood sample for complete blood count and biochemical analysis.

10. If the mare continues to deteriorate, serious consideration should be given to a fresh whole blood transfusion (). The main purpose of the transfusion is to provide more oxygen carrying red blood cells. Even though a conservative amount of anticoagulant is prescribed in this protocol, the risk that progression of clot formation could be hindered is always present. A vaccinated, equine infectious anemia-negative gelding or nonparous mare is a suitable donor.

The additional expense of the following adjunctive medications may be deemed necessary once the mare has stabilized:

1. Aminocaproic acid — a hemostatic agent to inhibit fibrinolysis; 20 g in fluids can be given as a loading dose, followed by 10 g every 6 hours thereafter; usually started if mare is stabilized, because clot fibrinolysis should not begin until 12 hours after its formation.

2. Flunixin meglumine — -to control inflammation and endotoxin insult; follow appropriate dosage and regimen.

3. Furosemide — to promote enhanced renal blood flow in the face of aggressive resuscitation; follow appropriate dosage and regimen.

4. Various tranquilizers — to calm uncontrollable mares; this author avoids these and has not found one to be better than another. A sudden drop in blood pressure may occur in a hypovolemic mare.

5. Broad-spectrum antibiotics — sulfonamides or penicillin/gentamicin strongly encouraged if the mare is hydrated.

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Placental Hydrops

Hydrops is a rare condition in the mare, with hydroallantois occurring more commonly than hydramnios. Hydroallantois causes rapid abdominal enlargement during the last trimester of pregnancy (), and a sudden increase in the volume of allantoic fluid during a period of 10 to 14 days. The pathophysiology of hydroallantois in the mare remains unknown. Some authors have suggested that the increase in fluid is a placental problem caused either by increased production of fluid or decreased transplacental absorption. Others have proposed that the etiology is related to placentitis and heritability. In these authors’ experience, examination of the fetus and fetal membranes have rarely demonstrated any consistent abnormality. One mare had diffuse mild placentitis (with leptospirosis) and another had histologic evidence of vasculitis when an endometrial biopsy was taken within 2 days of delivery of the fetus.

Mares may present with anorexia, tachycardia, severe ventral edema/plaques, abdominal discomfort, and labored breathing caused by pressure on the diaphragm. They typically have difficulty walking and often become recumbent. Uterine rupture may occur in advanced cases. Other complications associated with the excessive weight of the uterine contents include prepubic tendon rupture and development of abdominal wall and inguinal hernias.

Rectal palpation is diagnostic and reveals a huge, taut, fluid-filled uterus. The fetus cannot be balloted. Transrectal ultrasound imaging shows hyperechogenic allantoic fluid. The fetus is seldom observed as a result of the depth of the enlarged uterus. Transabdominal ultrasound will confirm the presence of excessive echogenic allantoic fluid and this approach does permit evaluation of fetal viability (movement and a heart rate of 80-100 bpm).

Treatment of Placental Hydrops

During the last few years the medical facility at these authors’ clinic has seen an increase in the number of hydroallantois cases presented to the clinic. Once the diagnosis of hydroallantois is confirmed, fetal viability is determined, and udder development and the milk electrolytes are assessed to estimate the level of fetal maturity. Those mares that present early in gestation may undergo elective termination of pregnancy by IM injection of cloprostenol (500 μg, 2 ml IM ql2h until delivery). Cases that occur later in gestation, or those with profound abdominal enlargement, may have large volumes of fluid within the uterus and require controlled drainage of the fluid before expulsion of the fetus. The reason for the controlled drainage is that excessive uterine distention alters total body fluid balance and venous return to the right heart. Sudden loss of this large volume of fluid may result in hypovolemic shock. The effect of the fluid loss is exacerbated by the sudden expansion of the abdominal venous circulation once the uterine weight is reduced. In the short term, abdominal support (i.e., belly band), IV fluids, steroids, broad-spectrum antibiotics, and antiinflammatory medication will provide systemic support for the mare. Slow siphoning of the allantoic fluid is then attempted. Once the size of the distended uterus has been reduced, the authors have used oxytocin (20 IU IV given repeatedly or 50 IU in a saline drip) or cloprostenol (two doses of 500 μg, 30 minutes apart) to promote fetal expulsion. In these authors’ experience, cloprostenol has provided a smooth progression of labor, with stage 2 occurring 30 to 60 minutes after the second dose. Mares that present within the last 2 to 4 weeks of pregnancy may be managed by partial drainage. The aim in these cases is to maintain the pregnancy for as long as possible in order for additional fetal maturation to occur.

The technique for drainage involves several considerations. Location (stocks or stall) is determined by individual preference and the condition of the mare. The process takes 2 to 3 hours, so comfort is a factor. The clinician should initiate supportive care by placing an IV catheter and administering a slow infusion of a crystalloid fluid. A tail wrap and sterile surgical preparation of the mare’s perineum is essential. The equipment includes a 24- to 32-French sharp thoracic trocar catheter, a two-way plastic adapter, sterile plastic tubing, a sterile sleeve, and buckets to collect the allantoic fluid. Smaller-sized catheters will take longer for fluid removal. The technique involves sterile passage of the catheter through the vagina and cervix, and sharp puncture of the chorioallantois. The sharp trocar is removed and the two-way adapter is used to connect the catheter to the tubing. The catheter is held in place by the clinician’s arm within the vagina. Controlled gradual drainage can then be performed into the buckets. Some pericervical separation of the placenta is common.

Several mares have been successfully treated in these authors’ hospital with this technique. In a few cases (6) that were within 2 to 4 weeks of term, maintenance of the pregnancy has been attempted after partial drainage of the allantoic compartment. These mares were treated with additional antimicrobial therapy, antiinflammatory medications (flunixin meglumine, pentoxifylline), agents with possible tocolytic activity (isoxsuprine, clenbuterol, albuterol), and altrenogest. In cases where partial drainage is attempted, fetal death may occur as a result of fetal asphyxia that results from varying degrees of placental separation. Iatrogenic fetal infection, secondary to contamination of the placental fluids during drainage, is also a problem. In most cases attempted to date, the fetus has become infected with Escherkhia coli and subsequently died. One mare died after 72 hours as a result of rupture of a uterine artery. The fetus in that mare had remained alive and exhibited normal parameters when monitored by transabdominal ultrasound.

Owners should be advised that the fetus is usually lost in mares with hydroallantois. However, early recognition of the problem, and prompt intervention, provides a good prognosis for the mare both physically and reproductively. Complications that should be anticipated when managing a mare with hydroallantois include hypovolemic shock, dystocia, and retention of the fetal membranes. The hypovolemia requires rapid volume expansion with use of large volume crystalloid infusion (as high as 40 ml/kg) alone, or in combination with hypertonic saline (4 ml/kg). The use of colloid fluids such as hetastarch (10 ml/kg) might also be beneficial. Dystocia may be associated with incomplete cervical dilation and uterine inertia. Malpositioning and malpostures are common. Therefore manual assistance to deliver the foal is necessary. Management of retained fetal membranes is discussed elsewhere in this text (see “Retained Fetal Membranes”). Because it is possible that a heritable component to this condition exists, breeding to a different stallion may be prudent.

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Placentitis

The equine placenta consists of the allantochorion, the allantoamnion, and the umbilical cord. The chorionic portion of the allantochorion is attached to the endometrium by microcotyledons that are present throughout the uterus, with the exception of a small area at the internal os of the cervix called the cervical star. The allantochorion supports the fetus in utero. This structure provides respiratory and nutrient exchange between the mare and the fetus and is an endocrine organ for maintenance and normal development of the fetus. The “free floating” allantoamnion allows the fetus to move freely within the uterus. The only attachment between the fetus and the allantoamnion is at the umbilicus. The umbilicus contains two umbilical arteries, one umbilical vein, and the urachus. The length of the cord and the length of the allantoic and amniotic portions can vary, but is normally 50 to 100 cm long.

Pregnancy loss during late gestation can be the result of fetal illness, placental dysfunction, maternal illness, or a combination of these factors. A functional placenta is necessary for a normal development of the fetus. Any insult or disruption of normal anatomy or physiology of the placenta may result in placental insufficiency and abortion. Compromised placental anatomy or function is the most common cause of abortions in late gestational mares. Placental insufficiency may be noninfectious (e.g., twin pregnancy) or infectious. Effective management of twin pregnancies has reduced this cause of abortion, and placentitis has become one of the most common cause of abortion in late gestational mares.

Placentitis: Etiology

The most common route of infection is believed to be ascension through the cervix. An ascending infection may be the result of a failure of the external genital barriers to protect the uterus from bacterial or fungal invasion (e.g., defective perineal conformation, nonfunctional vestibulovaginal fold, or cervical lacerations). The possibility of bacterial contamination entering the uterus at the time of breeding or the presence of a preexisting low-grade endometritis with clinical signs that develop several months later has not been critically investigated. The characteristic location of the lesions away from the cervix in mares with placentitis caused by a Nocardioform actinomycete raises the question of whether the microorganism may enter the uterus before, or at the time of breeding, without causing a clinical problem until later during the pregnancy. Hematogenously spread placentitis occurs but is considered to be less common than an ascending route of infection.

The most commonly isolated microorganisms from mares with placentitis are Streptococcus zooepidemicus, Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, Nocardioform actinomycete, Aspergillus spp., and Candida organisms. The mechanism of abortion as a result of placentitis is not fully understood, but it most likely involves infection of the fetus, hormonal changes, the release of inflammatory mediators, and deprivation of the fetus of nutrients.

Placentitis: Clinical Signs and Diagnosis

Placentitis: Treatment And Prevention

Treatment of mares with placentitis should focus on elimination of the infectious agents, reduction of the inflammatory response, and reduction of the increased myometrial contractility in response to the ongoing inflammation. No controlled studies have been reported on the efficacy of treatments for mares with placentitis, and the following recommendations are based on clinical experience and extrapolation from other species.

Urine pooling, cervical lesions, and poor perineal conformation should be corrected to prevent an ascending route of infection during pregnancy. Mares with abnormal placental findings on ultrasonographic examination or clinical signs of placentitis should be treated with broad-spectrum antibiotics, antiinflammatories (flunixin meglumine, 1.1 mg/kg ql2h; or phenylbutazone, 4 mg/kg ql2h), and tocolytics (altrenogest, 0.088 mg/kg q24h; or clenbuterol, 0.8 μg/kg ql2h). Pentoxifylline (7.5 mg/kg PO ql2h) is thought to increase oxygenation of the placenta through an increased deformability of red blood cells. A bacterial culture should be obtained in mares with vaginal discharge for isolation of a causative agent and sensitivity to antibiotics. After foaling or abortion, the uterus of the mare should be cultured and the mare should be treated for endometritis if the culture is positive.

Mares have been reported to deliver normally developed foals several weeks or even months after successful treatment of placentitis. No current diagnostic method exists, however, to predict how the compromised uterine environment in a mare with placentitis will affect the development of her fetus in individual cases.